Long non-coding RNA UPAT promotes cell proliferation via regulating the miR-133a/IGF1R axis in colorectal cancer

Many long noncoding RNAs (lncRNAs) are dysregulated in human cancers and play critical roles in tumor development and progression. It has been reported that long noncoding RNA UPAT promotes colon tumorigenesis by inhibiting degradation of UHRF1. However, the function and molecular mechanism of UPAT in colorectal cancer (CRC) needs to be further studied. In this study, we found that UPAT expression was inversely correlated to miR-133a expression in colorectal cancer tissues and cells. In addition, knockdown of UPAT inhibited cell proliferation and cell cycle progression of colorectal cancer. Further mechanistic studies revealed that UPAT could sponge endogenous miR-133a and inhibit its activity. Moreover, both UPAT knockdown and miR-133a overexpression in CRC cell lines led to cell proliferation and cell cycle progression was inhibited. We also found that insulin-like growth factor 1 receptor (IGF1R), a known target of miR-133a, was inhibited by both UPAT knockdown and miR-133a overexpression. Furthermore, tumor growth suppression was retarded with miR-133a down-regulated in UPAT knockdown of colorectal cancer cells xenografts. Taken together, our work provides the first evidence of a UPAT-miR-133a-IGF1R regulatory network in CRC and reveals that UPAT is a potential new oncogene for CRC.